Temporal changes in plasma membrane lipid content induce endocytosis to regulate developmental epithelial-to-mesenchymal transition

2020 ◽  
Author(s):  
Glòria Casas Gimeno
Keyword(s):  
Plasma Membrane ◽  
Lipid Content ◽  
Epithelial To Mesenchymal Transition ◽  
Membrane Lipid ◽  
Temporal Changes ◽  
Mesenchymal Transition ◽  
Plasma Membrane Lipid

scholarly journals Temporal changes in plasma membrane lipid content induce endocytosis to regulate developmental epithelial-to-mesenchymal transition

2020 ◽  
Author(s):  
Michael L. Piacentino ◽  
Erica J. Hutchins ◽  
Cecelia J. Andrews ◽  
Marianne E. Bronner
Keyword(s):  
Gene Expression ◽  
Plasma Membrane ◽  
Neural Crest ◽  
Lipid Content ◽  
Epithelial To Mesenchymal Transition ◽  
Membrane Lipid ◽  
Bmp Signaling ◽  
Membrane Function ◽  
Mesenchymal Transition ◽  
Plasma Membrane Lipid

AbstractEpithelial-to-mesenchymal transition (EMT) is a dramatic change in cellular physiology during development and metastasis which involves coordination between cell signaling, adhesion, and membrane protrusions. These processes all involve dynamic changes in the plasma membrane, yet how membrane lipid content regulates membrane function during developmental EMT remains incompletely understood. By screening for differential expression of lipid-modifying genes over the course of EMT in avian neural crest, we have identified the ceramide-producing enzyme neutral sphingomyelinase 2 (nSMase2) as a critical regulator of a developmental EMT. nSMase2 expression begins at the onset of EMT, and in vivo knockdown experiments demonstrate that nSMase2 is necessary for neural crest migration. Further, we find that nSMase2 promotes Wnt and BMP signaling, and is required to activate the mesenchymal gene expression program. Mechanistically, we show that nSMase2 is sufficient to induce endocytosis, and that inhibition of endocytosis mimics nSMase2 knockdown. Our results support a model in which nSMase2 is expressed at the onset of neural crest EMT to produce ceramide and induce membrane curvature, thus increasing endocytosis of Wnt and BMP signaling complexes and activating pro-migratory gene expression. These results highlight the critical role of plasma membrane lipid metabolism in regulating transcriptional changes during developmental EMT programs.

scholarly journals Deciphering the Importance of Glycosphingolipids on Cellular and Molecular Mechanisms Associated with Epithelial-to-Mesenchymal Transition in Cancer

Biomolecules ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 62
Author(s):  
Cécile Cumin ◽  
Yen-Lin Huang ◽  
Arun Everest-Dass ◽  
Francis Jacob
Keyword(s):  
Cell Surface ◽  
Molecular Mechanisms ◽  
Epithelial To Mesenchymal Transition ◽  
Membrane Integrity ◽  
Tumor Development ◽  
Membrane Lipid ◽  
Mesenchymal Transition ◽  
Mesenchymal To Epithelial Transition ◽  
Plasma Membrane Lipid ◽  
Metastatic Sites

Every living cell is covered with a dense and complex layer of glycans on the cell surface, which have important functions in the interaction between cells and their environment. Glycosphingolipids (GSLs) are glycans linked to lipid molecules that together with sphingolipids, sterols, and proteins form plasma membrane lipid rafts that contribute to membrane integrity and provide specific recognition sites. GSLs are subdivided into three major series (globo-, ganglio-, and neolacto-series) and are synthesized in a non-template driven process by enzymes localized in the ER and Golgi apparatus. Altered glycosylation of lipids are known to be involved in tumor development and metastasis. Metastasis is frequently linked with reversible epithelial-to-mesenchymal transition (EMT), a process involved in tumor progression, and the formation of new distant metastatic sites (mesenchymal-to-epithelial transition or MET). On a single cell basis, cancer cells lose their epithelial features to gain mesenchymal characteristics via mechanisms influenced by the composition of the GSLs on the cell surface. Here, we summarize the literature on GSLs in the context of reversible and cancer-associated EMT and discuss how the modification of GSLs at the cell surface may promote this process.

Dietary fat ratios and liver plasma membrane lipid composition

Lipids ◽  
1988 ◽  
Vol 23 (9) ◽  
pp. 829-833 ◽  
Author(s):  
Michael W. Hamm ◽  
Anna Sekowski ◽  
Roni Ephrat
Keyword(s):  
Plasma Membrane ◽  
Lipid Composition ◽  
Dietary Fat ◽  
Membrane Lipid ◽  
Membrane Lipid Composition ◽  
Liver Plasma Membrane ◽  
Plasma Membrane Lipid

Alterations in plasma membrane lipid organization during lymphocyte differentiation

1986 ◽  
Vol 126 (3) ◽  
pp. 379-388 ◽  
Author(s):  
Brian J. Del Buono ◽  
Patrick L. Williamson ◽  
Robert A. Schlegel
Keyword(s):  
Plasma Membrane ◽  
Membrane Lipid ◽  
Lymphocyte Differentiation ◽  
Plasma Membrane Lipid ◽  
Lipid Organization

1P-0227 Apolipoprotein A-1 interaction with plasma membrane lipid rafts controls cholesterol export from macrophages

2003 ◽  
Vol 4 (2) ◽  
pp. 69 ◽  
Author(s):  
W. Jessup ◽  
K. Gaus ◽  
L. Kritharides ◽  
A. Boettcher ◽  
W. Drobnik ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Lipid Rafts ◽  
Membrane Lipid ◽  
Apolipoprotein A ◽  
Plasma Membrane Lipid

Time-Course of Changes in the Plasma–Membrane Lipid Bilayer and Cellular Ultrastructure Induced by Tumour Necrosis Factor-α in K 562 and Daudi Cells

1995 ◽  
Vol 23 (4) ◽  
pp. 254-263 ◽  
Author(s):  
M Marutaka ◽  
H Iwagaki ◽  
K Mizukawa ◽  
N Tanaka ◽  
K Orita
Keyword(s):  
Plasma Membrane ◽  
Cell Membrane ◽  
Membrane Fluidity ◽  
Time Course ◽  
Membrane Lipid ◽  
Plasma Membrane Lipid ◽  
Membrane Lipid Bilayer ◽  
Cell Membrane Fluidity ◽  
K 562 Cells ◽  
Factor Α

The time-course of changes in the plasma-membrane lipid bilayer induced by tumour necrosis factor-α (TNF) were investigated in cultured cells using spin-label electron-spin-resonance techniques. Treatment of K 562 cells, a human chronic myelocytic leukaemia cell line, in suspension culture with TNF for up to 6 h caused an initial increase in cell-membrane fluidity, which returned to the control level after 12 h of treatment. After 24 h of treatment, the cell-membrane fluidity had decreased and this decrease was maintained after 48 h of treatment. In Daudi cells, a human malignant lymphoma cell line, TNF, did not induce any changes in cell-membrane fluidity, indicating that the effect of TNF on membrane structure is cell-specific. The early and transient change in membrane fluidity in K 562 cells is probably related to signal generation, while the later, persistent change may reflect the phenotype of TNF-treated cells, in particular, changes in the plasma membrane-cytoplasmic complex. Histochemical electron microscopic studies indicated that the membrane fluidity changes induced by TNF have an ultrastructural correlate.

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